title: Morphostasis: an evolving perspective.
abstract: In an earlier article, I proposed a pathway by which morphostasis (tissue homeostasis) may have evolved. It began in single-celled organisms and culminated in the mammalian immune system. This evolutionary path is now traced from its source--the intracellular surveillance within an isolated cell of its own internal health. Morphostasis sequentially incorporates heat shock proteins, apoptosis, cell adhesion molecules, complement components, gap junctions, phagocytes, natural killer cells, cytotoxic T-cells, helper cells and antibodies. I propose that the sequence leading to the insertion of gap junctions is an ancestor of the complement attack sequence. Although contentious, this deduction is intriguing, since numerous, minimal clues support the proposition. The broad hypothesis emphasizes a theme that may prove to be a useful framework on which to hang a better understanding of immunology and embryology. It highlights points where a concentrated research effort may rapidly advance our understanding of both.
authors.affiliation: Waterside Health Centre, Hythe, Southampton. jamie_cunliffe@msn.com
authors.forename: J
authors.initials: J
authors.lastname: Cunliffe
mesh_terms: D000818:Animals; D005075:Biological Evolution; D015815:Cell Adhesion Molecules / Q000502:physiology; D003165:Complement System Proteins / Q000502:physiology; D017629:Gap Junctions / Q000502:physiology; D006360:Heat-Shock Proteins / Q000378:metabolism; D006706:Homeostasis; D006801:Humans; D008214:Lymphocytes / Q000276:immunology*; D008954:Models, Biological; D010586:Phagocytes / Q000502:physiology
chemical_list: D015815:Cell Adhesion Molecules; D006360:Heat-Shock Proteins; D003165:Complement System Proteins